Since tumor promoters are nonnutagenic and membrane active, one hypothesis for the mechanism of tumor promotion proposes that the biological response is mediated by specific promoter-induced changes in cell surface glycoconjugate targets. Recent investigations in our laboratory have led to the discovery of three promoter-sensitive glycoproteins in JB6 cells having molecular weights 180,000, 150,000, and 220,000. The gp180 ad gp150 have been identified as the pro-alpha-1 and pro-alpha-2 subunits of procollagen, respectively. Both phorbol and non-phorbol promoters such as epidermal growth factor and mezerein are active in producing these 3 glycoprotein decreases. TPA exposure switches off procollagen synthesis pretranslationlly (probably transcriptionally) as indicated by a lack of translatable collagen mRNA assayed in an in vitro protein synthesis system. Antipromoting concentrations of retinoic acid prevent the decreases in procollagen levels produced propose that the transcriptional switch affecting collagen synthesis is indicative of a required event in promotion which is coordinately regulated with procollagen.